Loss of sphingosine kinase 2 protects against cisplatin-induced kidney injury

Xie, Dengpiao; Hu, Gaizun; Chen, Chaoling; Ahmadinejad, Fereshteh; Wang, Weili; Li, Pin‐Lan; Gewirtz, David A.; Li, Ningjun

doi:10.1152/ajprenal.00229.2021

Cited by 5 publications

(4 citation statements)

References 85 publications

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“…The public single cell datasets from the Humphreys’ lab 1 suggests that Bst1 is abundantly expressed in distal tubule and its expression is enhanced at 12 h after renal ischemia-reperfusion injury ( 50 ). Furthermore, there is a report that blocking Sphk2, which is highly expressed in the proximal tubules, improved cisplatin-induced nephropathy ( 51 ), suggesting that Bst1 may be related to other factors besides fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Bone marrow stromal cell antigen-1 (CD157) regulated by sphingosine kinase 2 mediates kidney fibrosis

Inoue

Nakamura²,

Tanaka³

et al. 2022

Front. Med.

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Chronic kidney disease is a progressive disease that may lead to end-stage renal disease. Interstitial fibrosis develops as the disease progresses. Therapies that focus on fibrosis to delay or reverse progressive renal failure are limited. We and others showed that sphingosine kinase 2-deficient mice (Sphk2–/–) develop less fibrosis in mouse models of kidney fibrosis. Sphingosine kinase2 (SphK2), one of two sphingosine kinases that produce sphingosine 1-phosphate (S1P), is primarily located in the nucleus. S1P produced by SphK2 inhibits histone deacetylase (HDAC) and changes histone acetylation status, which can lead to altered target gene expression. We hypothesized that Sphk2 epigenetically regulates downstream genes to induce fibrosis, and we performed a comprehensive analysis using the combination of RNA-seq and ChIP-seq. Bst1/CD157 was identified as a gene that is regulated by SphK2 through a change in histone acetylation level, and Bst1–/– mice were found to develop less renal fibrosis after unilateral ischemia-reperfusion injury, a mouse model of kidney fibrosis. Although Bst1 is a cell-surface molecule that has a wide variety of functions through its varied enzymatic activities and downstream intracellular signaling pathways, no studies on the role of Bst1 in kidney diseases have been reported previously. In the current study, we demonstrated that Bst1 is a gene that is regulated by SphK2 through epigenetic change and is critical in kidney fibrosis.

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Section: Discussionmentioning

confidence: 99%

Bone marrow stromal cell antigen-1 (CD157) regulated by sphingosine kinase 2 mediates kidney fibrosis

Inoue

Nakamura²,

Tanaka³

et al. 2022

Front. Med.

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“…On Day 3 and Day 6, 10% MTS was then added to the culture medium and incubated at 37°C for 4 hours. The absorbance was measured at the wavelengths 490 nm (Xie et al, 2022).…”

Section: The Inhibitory Effects Of Faah Inhibition and Cisplatin In C...mentioning

confidence: 99%

“…Clonogenic survival assay was performed as previously described (Ahmadinejad et al, 2022;Xie et al, 2022). Cells were seeded at a low density (1 x 10 2 HN12 in 6-well plates or 5 x 10 2 HN30 in 10 cm dishes), and exposed to 5 µM cisplatin in the absence and presence of 1 µM PF-04457845.…”

Section: Toxicity Of Cisplatin and Faah Inhibition On Cancer Cells By...mentioning

confidence: 99%

“…Nuclear factor-κB (NF-κB) p65 subunit is a key transcription factor that regulates inflammasome activation (Lawrence, 2009). Cisplatin is known to induce nuclear translocation of NF-κB p65 from the cytoplasm (Yeh et al, 2004;Xie et al, 2022), which is a critical step in producing many inflammatory cytokines as well as caspase-1-Interleukin (IL)-1β inflammasome activation (Lawrence, 2009;Lamkanfi and Dixit, 2014).…”

Section: Faah Knockout Mice Are Protected From Cisplatin-induced Nucl...mentioning

confidence: 99%

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Genetic Knockout of Fatty Acid Amide Hydrolase Ameliorates Cisplatin-Induced Nephropathy in Mice

Chen¹,

Wang²,

Raymond³

et al. 2023

Mol Pharmacol

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Cisplatin is a potent first-line therapy for many solid malignancies such as breast, ovarian, lung, testicular and head and neck cancer. However, acute kidney injury (AKI) is a major dose-limiting toxicity in cisplatin therapy, which often hampers the continuation of cisplatin treatment. The endocannabinoid system, consisting of anandamide (AEA) and 2-arachidonoylglycerol and cannabinoid receptors, participates in different kidney diseases. Inhibition of fatty acid amide hydrolase (FAAH), the primary enzyme for the degradation of AEA and AEA-related N-acylethanolamines, elicits antiinflammatory effects; however, little is known about its role in cisplatin nephrotoxicity.The current study tested the hypothesis that genetic deletion of Faah mitigates cisplatininduced AKI. Male wild-type C57BL6 (WT) and Faah −/− mice were administered a single dose of intraperitoneal injection of cisplatin (30 mg/kg) and euthanatized 72 hours later.Faah −/− mice showed a reduction of cisplatin-induced blood urea nitrogen, plasma creatinine levels, kidney injury markers and tubular damage in comparison with WT mice. The renal protection from Faah deletion was associated with enhanced tone of AEA-related N-acylethanolamines (PEA and OEA), attenuated NF-κB/p65 activity, DNA damage markers p53, p21 and decreased expression of the inflammatory cytokine IL-1β as well as infiltration of macrophages and leukocytes in the kidneys. Notably, a selective FAAH inhibitor (PF-04457845) did not interfere with or perturb the antitumor effects of cisplatin in two head and neck squamous cell carcinoma cell lines, HN30 and HN12. Our work highlights that FAAH inactivation prevents cisplatin-induced nephrotoxicity in mice and that targeting FAAH could provide a novel strategy to mitigate cisplatin-induced nephrotoxicity.

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Molecular mechanism of ion channel protein TMEM16A regulated by natural product of narirutin for lung cancer adjuvant treatment

Shi

Bai

et al. 2022

International Journal of Biological Macromolecules

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Loss of sphingosine kinase 2 protects against cisplatin-induced kidney injury

Cited by 5 publications

References 85 publications

Bone marrow stromal cell antigen-1 (CD157) regulated by sphingosine kinase 2 mediates kidney fibrosis

Bone marrow stromal cell antigen-1 (CD157) regulated by sphingosine kinase 2 mediates kidney fibrosis

Genetic Knockout of Fatty Acid Amide Hydrolase Ameliorates Cisplatin-Induced Nephropathy in Mice

Molecular mechanism of ion channel protein TMEM16A regulated by natural product of narirutin for lung cancer adjuvant treatment

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